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Transcript
Congestive Heart Failure
Michele Ritter, M.D.
Argy – February, 2007
Heart Failure

Results from any structural or
functional abnormality that impairs
the ability of the ventricle to eject
blood (Systolic Heart Failure) or
to fill with blood (Diastolic Heart
Failure).
The Vicious Cycle of Congestive Heart
Failure
LV Dysfunction causes
Decreased cardiac output
Decreased Blood Pressure and
Decreased Renal perfusion
Stimulates the Release
of renin, Which allows
conversion of
Angiotensin
to Angiotensin II.
Angiotensin II stimulates
Aldosterone secretion which
causes retention of
Na+ and Water,
increasing filling pressure
Types of Heart Failure

Low-Output Heart Failure

Systolic Heart Failure:



Diastolic Heart Failure:



Elevated Left and Right ventricular end-diastolic
pressures
May have normal LVEF
High-Output Heart Failure



decreased cardiac output
Decreased Left ventricular ejection fraction
Seen with peripheral shunting, low-systemic vascular
resistance, hyperthryoidism, beri-beri, carcinoid, anemia
Often have normal cardiac output
Right-Ventricular Failure

Seen with pulmonary hypertension, large RV infarctions.
Causes of Low-Output Heart Failure

Systolic Dysfunction


Coronary Artery Disease
Idiopathic dilated cardiomyopathy (DCM)






50% idiopathic (at least 25% familial)
9 % mycoarditis (viral)
Ischemic heart disease, perpartum, hypertension,
HIV, connective tissue disease, substance abuse,
doxorubicin
Hypertension
Valvular Heart Disease
Diastolic Dysfunction




Hypertension
Coronary artery disease
Hypertrophic obstructive cardiomyopathy (HCM)
Restrictive cardiomyopathy
Clinical Presentation of Heart Failure

Due to excess fluid accumulation:






Dyspnea (most sensitive symptom)
Edema
Hepatic congestion
Ascites
Orthopnea, Paroxysmal Nocturnal Dyspnea
(PND)
Due to reduction in cardiac ouput:


Fatigue (especially with exertion(
Weakness
Physical Examination in Heart Failure

S3 gallop


Cool, pale, cyanotic extremities








Low sensitivity, but highly specific
Have sinus tachycardia, diaphoresis and peripheral
vasoconstriction
Crackles or decreased breath sounds at bases
(effusions) on lung exam
Elevated jugular venous pressure
Lower extremity edema
Ascites
Hepatomegaly
Splenomegaly
Displaced PMI

Apical impulse that is laterally displaced past the
midclavicular line is usually indicative of left ventricular
enlargement>
Measuring Jugular Venous Pressure
Lab Analysis in Heart Failure

CBC


Serum electrolytes and creatinine




To evaluate for possible diabetes mellitus
Thyroid function tests


before starting high dose diuretics
Fasting Blood glucose


Since anemia can exacerbate heart failure
Since thyrotoxicosis can result in A. Fib,
and hypothyroidism can results in HF.
Iron studies

To screen for hereditary hemochromatosis as cause of heart
failure.

To evaluate for possible lupus
ANA
Viral studies

If viral mycocarditis suspected
Laboratory Analysis (cont.)

BNP


With chronic heart failure, atrial mycotes
secrete increase amounts of atrial natriuretic
peptide (ANP) and brain natriuretic pepetide
(BNP) in response to high atrial and
ventricular filling pressures
Usually is > 400 pg/mL in patients with
dyspnea due to heart failure.
Chest X-ray in Heart Failure




Cardiomegaly
Cephalization of the pulmonary
vessels
Kerley B-lines
Pleural effusions
Cardiomegaly
Pulmonary vessel congestion
Pulmonary Edema due to Heart Failure
Kerley B lines
Cardiac Testing in Heart Failure

Electrocardiogram:

May show specific cause of heart
failure:





Ischemic heart disease
Dilated cardiomyopathy: first degree AV
block, LBBB, Left anterior fascicular block
Amyloidosis: pseudo-infarction pattern
Idiopathic dilated cardiomyopathy: LVH
Echocardiogram:


Left ventricular ejection fraction
Structural/valvular abnormalities
Further Cardiac Testing in Heart Failure

Exercise Testing


Should be part of initial evaluation of all patients
with CHF.
Coronary arteriography



Should be performed in patients presenting with
heart failure who have angina or significant
ischemia
Reasonable in patients who have chest pain that
may or may not be cardiac in origin, in whom
cardiac anatomy is not known, and in patients with
known or suspected coronary artery disease who do
not have angina.
Measure cardiac output, degree of left ventricular
dysfunction, and left ventricular end-diastolic
pressure.
Further testing in Heart Failure

Endomyocardial biopsy
Not frequently used
 Really only useful in cases such as viralinduced cardiomyopathy

Classification of Heart Failure

New York Heart Association (NYHA)




Class I – symptoms of HF only at
levels that would limit normal
individuals.
Class II – symptoms of HF with
ordinary exertion
Class III – symptoms of HF on less
than ordinary exertion
Class IV – symptoms of HF at rest
Classification of Heart Failure (cont.)

ACC/AHA Guidelines




Stage A – High risk of HF, without
structural heart disease or symptoms
Stage B – Heart disease with
asymptomatic left ventricular
dysfunction
Stage C – Prior or current symptoms
of HF
Stage D – Advanced heart disease and
severely symptomatic or refractory HF
Chronic Treatment of Systolic Heart
Failure

Correction of systemic factors





Lifestyle modification




Thyroid dysfunction
Infections
Uncontrolled diabetes
Hypertension
Lower salt intake
Alcohol cessation
Medication compliance
Maximize medications

Discontinue drugs that may contribute to heart
failure (NSAIDS, antiarrhythmics, calcium channel
blockers)
Order of Therapy
1.
2.
3.
4.
5.
6.
Loop diuretics
ACE inhibitor (or ARB if not
tolerated)
Beta blockers
Digoxin
Hydralazine, Nitrate
Potassium sparing diuretcs
Diuretics

Loop diuretics
Furosemide, buteminide
 For Fluid control, and to help relieve
symptoms


Potassium-sparing diuretics
Spironolactone, eplerenone
 Help enhance diuresis
 Maintain potassium
 Shown to improve survival in CHF

ACE Inhibitor


Improve survival in patients with all
severities of heart failure.
Begin therapy low and titrate up as
possible:
Enalapril – 2.5 mg po BID
 Captopril – 6.25 mg po TID
 Lisinopril – 5 mg po QDaily


If cannot tolerate, may try ARB
Beta Blocker therapy


Certain Beta blockers (carvedilol,
metoprolol, bisoprolol) can improve
overall and event free survival in NYHA
class II to III HF, probably in class IV.
Contraindicated:





Heart rate <60 bpm
Symptomatic bradycardia
Signs of peripheral hypoperfusion
COPD, asthma
PR interval > 0.24 sec, 2nd or 3rd degree block
Hydralazine plus Nitrates

Dosing:

Hydralazine


Isosorbide dinitrate


Started at 25 mg po TID, titrated up to 100
mg po TID
Started at 40 mg po TID/QID
Decreased mortality, lower rates of
hospitalization, and improvement in
quality of life.
Digoxin


Given to patients with HF to control
symptoms such as fatigue,
dyspnea, exercise intolerance
Shown to significantly reduce
hospitalization for heart failure, but
no benefit in terms of overall
mortality.
Other important medication in Heart
Failure -- Statins


Statin therapy is recommended in
CHF for the secondary prevention of
cardiovascular disease.
Some studies have shown a
possible benefit specifically in HF
with statin therapy
Improved LVEF
 Reversal of ventricular remodeling
 Reduction in inflammatory markers (CRP,
IL-6, TNF-alphaII)

Meds to AVOID in heart failure

NSAIDS


Thiazolidinediones



Can cause worsening of preexisting HF
Include rosiglitazone (Avandia), and
pioglitazone (Actos)
Cause fluid retention that can exacerbate HF
Metformin

People with HF who take it are at increased
risk of potentially lethic lactic acidosis
Implantable Cardioverter-Defibrillators
for HF



Sustained ventricular
tachycardia is associated with
sudden cardiac death in HF.
About one-third of mortality in
HF is due to sudden cardiac
death.
Patients with ischemic or
nonischemic cardiomyopathy,
NYHA class II to III HF, and
LVEF ≤ 35% have a significant
survival benefit from an
implantable cardioverterdefibrillator (ICD) for the
primary prevention of SCD.
Management of Refractory Heart
Failure

Inotropic drugs:


Mechanical circulatory support:



Dobutamine, dopamine, milrinone,
nitroprusside, nitroglycerin
Intraaortic balloon pump
Left ventricular assist device (LVAD)
Cardiac Transplantation



A history of multiple hospitalizations for HF
Escalation in the intensity of medical therapy
A reproducable peak oxygen consumption with
maximal exercise (VO2max) of < 14 mL/kg
per min. (normal is 20 mL/kg per min. or more)
is relative indication, while a VO2max < 10
mL/kg per min is a stronger indication.
Acute Decompensated Heart Failure


Cardiogenic pulmonary edema is a
common and sometimes fatal cause
of acute respiratory distress.
Characterized by the transudation of
excess fluid into the lungs
secondary to an increase in left
atrial and subsequently pulmonary
venous and pulmonary capillary
pressures.
Acute Decompensaated Heart Failure
(cont.)

Causes:

Acute MI


Volume Overload



Rupture of chordae tendinae/acute mitral
valve insufficiency
Transfusions, IV fluids
Non-compliance with diuretics, diet (high
salt intake)
Worsening valvular defect

Aortic stenosis
Decompensated Heart Failure

Symptoms



Severe dyspnea
Cough
Clinical Findings






Tachypnea
Tachycardia
Hypertension/Hypotension
Crackles on lung exam
Increased JVD
S3, S4 or new murmur
Labs/Studies in Acute Decompensated
Heart Failure





Chemistry, CBC
EKG
Chest X-ray
May consider cardiac enzymes
2D-Echo
Decompensated Heart Failure

Treatment






Strict I’s and O’s, daily weights
Oxygen, mechanical ventilation if
needed
Loop diuretics (Lasix!)
Morphine
Vasodilator therapy (nitroglycerin)
Nesiritide (BNP) – can help in acute
setting, for short term therapy
Case # 1

A 65-year old male with a history of
hypertension, DM, CAD s/p MI and threevessel CABG in 2002, presents with
worsening dyspnea on exertion. He
states that he occassionally has a dry
cough, but denies any recent chest pain,
fevers, N/V. Patient states that he usually
can get up a flight of stairs if he stops
half-way, but over the last several days,
has not been able to climb them at all.
Case # 1 (cont.)

PMH:





Allergies:


CAD – MI and CABG in 2002
Hypertension
Diabetes Mellitus
Hypothyroidism
NKDA
Outpatient Meds:



Synthroid
Metformin
Norvasc
Case # 1 (cont.)

Physical Exam:






97.6, 168/72, 99, 28, 93% on RA
Gen: Alert and oriented x 3, breathing
rapidly
CV: RRR, no murmurs; mod. JVD
Resp: Crackles throughout lungs
Abd.: soft, nontender, NABS
Ext: 2 + pitting edema bilaterally
Case # 1 (cont.)

Labs:







Hgb: 13.5
WBC: 8
Platelets: 240
Sodium: 139
Potassium: 3.8
BUN: 18
Cr: 0.8


Trop. I – 0.01
CPK: 120
Case # 1
Case # 1



What studies would you like to
check in this patient?
What medications would you like to
start/change?
What vital signs do you want to
monitor?
Case # 2

A 45-year old obese woman with diabetes
mellitus is evaluated for a 1-month
history of progressive shortness of
breath. Two months ago, she had a flulike illness with nausea, vomiting, and
sweating. She has not followed up with a
physician regularly. One of her siblings
has “heart problems” and her mother died
suddenly and unexpectedly at age 55
years.
Case # 2

On examination her heart rate is 75/min and her
blood pressure is 185/93 mm Hg. BMI is 32.9.
Jugular venous pressure is mildly elevated. Lung
examination reveals a few bibasilar crackles.
Cardiac examination reveals regular rhythm,
normal S1 and S2 and the presence of an S3.
There is mild peripheral edema. An
echocardiogram is significant for left ventricular
hypertrophy and severely decreased systolic
function (left ventricular ejection fraction, 20%)
An electrocardiogram shows a previous
anteroseptal MI.
Case # 2

(A)
(B)
(C)
(D)
(E)
Which of the following is the most
appropriate next diagnostic test?
Measurement of plasma BNP
Serum Protein Electrophoresis
Cardiac Stress Test
Cardiac catheterization
Endomyocardial biopsy